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Aim To investigate interinstitutional differences in preterm infant stabilisation between two European tertiary neonatal centres with particular focus on intubation timing, surfactant administration, caffeine therapy and neonatal morbidity and mortality. Methods Retrospective (2012‐2014) study of very low birth weight (VLBW) preterm infants admitted to John Radcliffe Hospital (UK centre) and Charité Medical Centre (German centre). Timing of intubation, surfactant and caffeine administration and respiratory outcomes were examined. Results Gestational age, birth weight and five‐minute Apgar scores of VLBW infants from the UK centre (n = 86) were comparable to those from the German centre (n = 96). Significant differences in antenatal steroid therapy, intubation timing and surfactant therapy were noted. Timing of caffeine initiation differed significantly between centres (median 0 [0‐2.5] UK vs. 2 [1.5‐4] days German centre); however, caffeine was discontinued at a similar corrected gestational age of 34.7 weeks. Mechanical ventilation was significantly longer at the UK centre, but there was no difference in bronchopulmonary dysplasia (BPD) (44% UK vs. 36% German centre) or mortality (15% UK vs. 13% German centre). Conclusion Timing of primary intubation and caffeine therapy differed significantly between centres. However, earlier intubation and caffeine administration in the UK centre were not associated with a changed incidence of BPD.

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with 20% FBS. In some experiments, cells were treated with TNF-a (10 ng/ml) and exposed to ACTZ (500 mM) or media buffered to pH 6.8. In other experiments, baseline differences between PASMC proliferation from 3 experimental groups (control, Sugen/Hypoxia or Sugen/Hypoxia+ACTZ animals) were compared. Cell numbers were evaluated with a haemochromocytometer using trypan blue cell exclusion 1, 2 and 3 after stimulation in triplicates. RT-qPCR was conducted to determine the expression of proliferative, contractile and dedifferentiation markers. Results RPASMCs exposed to TNF-a for 24 hours showed significant downregulation of markers of a contractile phenotype and upregulation of proliferative and de-differentiation markers. Exposure to TNF-a also resulted in increased proliferation, which was significantly reduced by exposure to ACTZ or acidosis. ACTZ or acidosis treatment also restored mRNA levels of contractile markers. Additionally, PASMCs isolated from control, SU/Hx and ACTZ-treated animals retained their respective phenotypes in vitro across a panel of markers. Subsequent to stimulation with 20% FBS, PASMCs of SU/Hx rats underwent significantly higher rates of proliferation, while cells from ACTZ-treated rats proliferated similarly to controls. Conclusion Acetazolamide partially restores RPASMC phenotypic switching and it may do so through induction of extracellular acidosis.

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